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Viruses 2015, 7(11), 5908-5918;

Antiviral Activity of Porcine Interferon Regulatory Factor 1 against Swine Viruses in Cell Culture

College of Animal Husbandry & Veterinary Science, Henan Agricultural University, Zhengzhou 450002, China
Author to whom correspondence should be addressed.
Academic Editor: Curt Hagedorn
Received: 7 September 2015 / Revised: 29 October 2015 / Accepted: 3 November 2015 / Published: 17 November 2015
(This article belongs to the Section Antivirals & Vaccines)
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Interferon regulatory factor 1 (IRF1), as an important transcription factor, is abundantly induced upon virus infections and participates in host antiviral immune responses. However, the roles of porcine IRF1 (poIRF1) in host antiviral defense remain poorly understood. In this study, we determined that poIRF1 was upregulated upon infection with viruses and distributed in nucleus in porcine PK-15 cells. Subsequently, we tested the antiviral activities of poIRF1 against several swine viruses in cells. Overexpression of poIRF1 can efficiently suppress the replication of viruses, and knockdown of poIRF1 promotes moderately viral replication. Interestingly, overexpression of poIRF1 enhances dsRNA-induced IFN-β and IFN-stimulated response element (ISRE) promoter activation, whereas knockdown of poIRF1 cannot significantly affect the activation of IFN-β promoter induced by RNA viruses. This study suggests that poIRF1 plays a significant role in cellular antiviral response against swine viruses, but might be dispensable for IFN-β induction triggered by RNA viruses in PK-15 cells. Given these results, poIRF1 plays potential roles in cellular antiviral responses against swine viruses. View Full-Text
Keywords: porcine IRF1; antiviral activity; IFN-β; IFN-stimulated genes porcine IRF1; antiviral activity; IFN-β; IFN-stimulated genes

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Li, Y.; Chang, H.; Yang, X.; Zhao, Y.; Chen, L.; Wang, X.; Liu, H.; Wang, C.; Zhao, J. Antiviral Activity of Porcine Interferon Regulatory Factor 1 against Swine Viruses in Cell Culture. Viruses 2015, 7, 5908-5918.

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